Movement Disorders
Vol. 8, No. 1, 1993, pp. 69-73
0 1993 Movement Disorder Society

Asymmetric Catalepsy After Right Hemisphere Stroke
Jeffrey L. Saver, *Penny Greenstein, "Michael Ronthal, and *M.-Marsel Mesulam
Department of Clinical Neurosciences, Rhode Island Hospital and Brown University, Providence, Rhode Island, and
*Department of Neurology, Beth Israel Hospital, Boston, Massachusetts, U.S.A.

Summary: We describe the appearance of left hemineglect and striking cataleptic posturing, more prominent in left-sided extremities, in a patient without
psychiatric illness. Neuroimaging demonstrated a large posterior right hemisphere infarct involving the parietal, occipital, and temporal lobes, the insula,
and caudate. Additional movement abnormalities that comprise the full catatonia syndrome were absent, including stereotypy, mannerisms, ambitendency , automatic obedience, mutism, negativism, and echopraxia. Catatonia
has been reported to be produced by lesions of diverse etiology affecting the
frontal lobe, limbic system, diencephalon, or basal ganglia. In these cases,
catalepsy has been manifest only rarely, and motor signs that are present are
generally bilateral. This case demonstrates that asymmetric catalepsy can be
produced by right hemisphere stroke, and provides partial support for earlier
clinical literature relating catalepsy and the parietal lobe. Key Words: Catalepsy-Waxy flexibility-Catatonia-Neglect-Parietal
lobe.

We describe a patient without psychiatric illness
who developed striking cataleptic posturing, more
prominent in left-sided extremities, after right hemisphere stroke.

Catalepsy denotes a tendency to maintain postures induced by the examiner (1,2). Of the varied
manifestations of the catatonic syndrome, catalepsy
is perhaps the most specific, and certainly the most
dramatic. Catatonia labels a cluster of psychomotor
symptoms and signs that may appear with idiopathic psychiatric disturbances, drug reactions,
metabolic derangements, and localized structural
lesions of the CNS (3,4). The classic features of
catatonia include mutism, stupor, catalepsy, negativism (including gegenhalten), mannerisms, stereotypy, bizarre postures, echolalia, echopraxia, automatic obedience, and catatonic excitement (furor)
(2,4). Among the idiopathic psychiatric disease
states, catatonia is more commonly associated with
affective disorder than with schizophrenia. Catalepsy is present in 20-30% of patients who exhibit
catatonia in association with an idiopathic psychiatric disturbance (5).

CASE REPORT

A 75-year-old, right-handed man presented with
complaints of clumsiness of the left hand and becoming lost in his house. There was no history of
psychiatric disease or exposure to neuroleptic
agents. The patient did not have known cardiac disease, nor major risk factors for atherothrombotic
stroke.
General medical examination results were unremarkable.
Mental status examination disclosed severe left
hemispatial neglect, constructional impairment,
spatial dysgraphia, difficulty with comprehension
and repetition of prosody, dressing difficulty, occasional hand-for-object substitutions bilaterally during execution of learned motor tasks, and inappropriate cheerfulness.
Elemental neurological examination demonstrated right gaze preference, and initial left hom-

A videotape segment accompanies this article.
Address correspondence and reprint requests to Dr. J. L.
Saver, 110 Lockwood Street, Suite 324, Providence, RI 02906,
U.S.A.

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J . L . SAVER ET AL.

onymous hemianopia, left hemihypoesthesia (dense
to pin and temperature, moderate to light touch),
minimally impaired left-sided vibration and joint
sense, and symmetric reflexes with flexor plantar
responses. There was minimal weakness of finger,
wrist, and elbow extension on the left, mild hypomimesis and some paucity of spontaneous movement, and no tremor. On testing for pronator drift,
the left arm moved upward minimally. Resting tone
was not elevated; tone increased with activation
more on the left than the right, without cogwheeling. The left hand was held in an abnormal posture
at rest, with flexion at the wrist. Dysmetria of finger-nose movements of the left hand was noted,
improving when the patient visualized the hand in
the right hemispace. Gait was slightly wide based,
with a tendency to circle toward the right; the left
hand maintained a dystonic posture during walking.
No grasp or avoiding reaction was noted.
Cataleptic posturing was noted, prominently in
the left upper extremity, to a lesser degree in the
right upper extremity and left lower extremity,
sparing the right lower extremity (Fig. 1). Without
prompting, the patient maintained postures produced by examiners’ positioning, even when uncomfortable, for up to 5 min. In addition, after completing a requested motion (e.g., holding arms up
for pronator drift testing) or a self-generated motion
(e.g., pointing), the patient would often maintain
the last posture of his movement for several minutes. The limbs would immediately release from
these sustained postures on further command from

the examiner or spontaneously if the patient employed the extremity for gesturation during free
conversation. When the posturing behavior of his
limbs was pointed out to him, he would state he had
not noticed they were in unusual positions. He
would then place the limbs in repose, but shortly
thereafter posturing would resume.
Waxy flexibility persisted with only slight diminution during the 7-day hospital course. Trials of
carbidopdlevodopa (Sinemet) and bromocriptine
produced no change in symptoms. At a follow-up
visit 2 weeks after onset, the patient’s family reported that they had observed unusual posturing at
home, especially of the left arm. For example, when
the patient rested from raking leaves, he was noted
to maintain the left arm in an unusual elevated posture for an extended period, thrusting the rake into
the air. The family stated that the patient had never
exhibited such behaviors before his stroke. At follow-up 1 year after onset, catalepsy could no longer
be elicited, although a tendency to maintain the left
hand in a flexed, dystonic posture was noted.
Acute cranial computed tomography scan and
follow-up cranial magnetic resonance scan obtained
6 days after symptom onset demonstrated infarction
in the posterior territories of the right middle cerebral artery (Fig. 2). Template analysis (6) disclosed
that the lesion primarily involved the right angular
and supramarginal gyri; the superior, middle, and
inferior temporal gyri; the posterior insula; and the
anterolateral occipital lobe (Fig. 3). A small infarct
in the body of the right caudate was also noted. An
electroencephalogram on hospital day 2 demonstrated continuous delta range slowing over the
right hemisphere, without epileptiform activity.
Etiologic workup failed to determine the source
of stroke.
DISCUSSION

FIG. 1. Photograph of patient maintaining postures induced by
the examiner during free conversation. Both upper extremities
and the left lower extremity show perseveration of posture. This
phenomenon could not be elicited from the right lower extremity.

Movement Disorders, V d . 8 , No. 1, 1993

There are more than 25 case reports in the literature of catatonia associated with focal brain injuries (2,4,7). Lesion sites most commonly are frontal, temporolimbic, o r subcortical (diencephalon,
basal ganglia, or brainstem), and are bilateral. Catalepsy is distinctly uncommon among these patients, and the catatonic motor signs that are present are generally symmetric. Three aspects of our
patient’s presentation are distinctive: (a) the appearance of catalepsy isolated from other signs of
the catatonia syndrome, (b) the asymmetry of cat-

ASYMMETRIC CATALEPSY

FIG. 2. Representative axial images from T2 signal-weighted
magnetic resonance imaging scan (relaxation time 2,500 ms, echo
time 80 ms), demonstrating infarction in the posterior territories
of the right middle cerebral artery. (Right side of images is right
side of brain.)

aleptic posturing, and (c) the association with a
well-documented unilateral parietotemporal injury.
Our patient did not exhibit the mental state
changes usually associated with catatonia, of either
the “excited” or “retarded” type. He also failed to
display classic motoric manifestations of catatonia
other than maintenance of posture. We suggest that
his condition represents an instance of catalepsy
sine catatonia. Catalepsy appearing in isolation in
this manner needs to be distinguished from a number of other pathologic motor phenomena.
The “perseveration of posture” of catalepsy differs from customary forms of motor perseveration.
The “inappropriate intrusion of a previous action or
response in ongoing activity” is the hallmark of
classic perseveration (8), often associated with
frontal systems injuries (9). Although several subtypes of perseverative behavior have been recognized (10,l I), all are characterized by the recurrent
performance of an action, as opposed to the persistence of posture after completion of an action or
after passive positioning seen in catalepsy. Cataleptic behavior also contrasts with akinetic-rigid syndromes of extrapyramidal origin and hypokinetichypometric syndromes seen after frontal and right

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hemisphere injury (12). In these, the preponderant
difficulties are with the initiation, speed, and gain of
movements. Difficulty with returning to rest after
completion of movement, if present, does not predominate.
The sustained persistence of posture seen in catalepsy may be viewed as a phenomenologic opposite of “motor impersistence,” the inability to sustain postures most commonly associated with frontal andlor right hemisphere lesions (13). Cataleptic
posturing with a parietal insult should also be distinguished from the “parietal hand” phenomenon.
The incoordination and dysmetria that can be associated with isolated parietal lesions has been reported to sometimes be accompanied by dystonic
posturing of the hand (14), but not persistence of
induced postures of multiple limbs.
One notable feature of our patient’s catalepsy
was its asymmetry, with perseveration of posture
more prominent in left-sided extremities, contralatera1 to the cerebral lesion. In reviewing the literature, we have not discovered previous reports of
strongly asymmetric catalepsy, with the exception
of a 19th-century account of the experimental induction of one-sided perseveration of posture in a
hypnotic subject (15).
Catatonic persistence of attitude has been associated with parietal lesions in rare case reports, but
generally without confirmation of localization by
modern neuroimaging techniques. Critchley , in his
monograph on the parietal lobe (16), listed among
features suggestive of parietal involvement in cases
of hemiparesis “a tendency towards the adoption of
catatonic-like postures by the affected upper limb.”
However, no report of particular cases accompanied this general observation. Denny-Brown and
Chambers, in their survey of parietal lobe function
(17), discussed cataleptic persistence of attitude as
an extreme manifestation of the “avoiding reaction”-a withdrawal response seen after parietal lesions analogous to the grasping reaction seen with
injuries to frontal cortices. They described briefly
one patient, a 59-year-old woman with a history of
presumed right parietal injury since the age of 15
years and a sudden new stroke producing additional
clinical signs of left parietal damage, whose limbs
“remained for many minutes in any posture passively applied to them.” No supportive neuroimaging or postmortem findings were available to confirm the clinical localization. Of note, DennyBrown and Chambers also reported experiments in
monkeys in which cataleptic posturing was pro-

Movement Disorders, Vol. 8 , N o . 1 , 1993

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J . L. SAVER ET AL.

7

FIG. 3. Template analysis of lesion based on
TI, proton density, and T2-weighted magnetic
resonance imaging sequences. The lesion primarily involved the angular and supramarginal
gyri, the superior, middle, and inferior temporal
gyri, the posterior insula, the anterolateral occipital lobe, and the body of the right caudate.

*
0

4

40

duced by surgical excision of parietal cortices. One
recent case with modern neuroimaging is also supportive of a link between parietal damage and persistence of posture: a full-blown catatonic syndrome, including catalepsy, was observed in association with bilateral parietal infarction (18).
Caution must be exercised in considering anatomic and physiologic bases for the cataleptic defect in our patient. The wide extent of his hemispheric infarction precludes precise anatomical localization. Moreover, postinfarction catalepsy is
rare, and middle cerebral artery infarcts are common, suggesting that an unusual combination of lesions and mechanisms, perhaps both extrapyramidal and cortical, are required to generate cataleptic
behavior. The collection of additional cases will
help to clarify these issues.
Nonetheless, several possibly complementary
mechanisms for the cataleptic defect in our patient
may be conjectured. One possibility is that our patient’s persistence of posture was the result of an
interaction of parietal neglect with hypokinesia of

Movement Disorders, Vol. 8 , No. 1, 1993

extrapyramidal origin. The literature on the modifying effects of supervening vascular lesions on the
manifestations of idiopathic Parkinson’s disease
and other akinetic-rigid syndromes is incomplete.
Pyramidal lesions are well known to cause disappearance or diminution of tremor during the period
of most severe weakness. Parkinson himself described the first such case (19). Infarctions of the
ventrolateral thalamus have acted as “vascular
thalamotomies’’ in parkinsonian patients, relieving
tremor and rigidity contralaterally (20). Similarly,
cerebellar infarction (21) and anterior choroidal artery occlusion (22) have been noted to abolish extrapyramidal rigidity and tremor. However, parietotemporal infarcts that spare primary motor systems
have not been systematically investigated in this regard. Our patient’s asymmetric catalepsy may have
been the collective product of a mild extrapyramidal hypokinetic syndrome modified by severe
asymmetric neglect from a posterior parietal infarction.
The entity of cortical-basal ganglionic degenera-

ASYMMETRIC CATALEPS Y

tion (CBGD) is often associated with asymmetric
limb rigidity and apraxia, in some instances resembling cataleptic posturing (23,24). Our patient exhibited a small lesion in the body of the right caudate. His ischemic cortical and subcortical injuries
may have compromised the same functional systems impaired by idiopathic degeneration in CBGD.
Against this potential mechanism, our patient did
not demonstrate the alien limb phenomenon, focal
myoclonus, postural-action tremor, and severe dystonia that patients with CBGD frequently develop,
and his isolated caudate injury spared many of the
subcortical sites typically affected in CBGD.
Another candidate mechanism recognizes that
frontal system lesions are frequently associated
with elements of the catatonic syndrome. Our patient’s lesions in the posterior insula, inferior parietal lobule, and a portion of primary somatosensory
cortex may have interrupted input from posterior to
anterior regions to a degree severe enough to produce functional deafferentation of frontal cortices.
Similarly, it may be noted that our patient’s lesions
involved posterolateral temporal cortices to a significant degree, and that temporal lesions have been
associated with the catatonic syndrome in several
cases. However, these patients generally differed
from ours in having bilateral rather than unilateral
lesions and in having prominent involvement of mesial-limbic temporal structures.
Studies of motor system physiology have been
primarily directed at analyzing functional elements
responsible for the planning, initiation, implementation, and ongoing feedback control of motor programs (25,26). Systems for recognizing the accurate
completion of a motor program and initiating a return to resting posture have not been well described. This case suggests that an important element of such a neural system may be localized in
parietotemporal cortices.

LEGENDS TO VIDEOTAPE
Segment 1. Moderate waxy flexibility while conversing with examiners.
Segment 2. Persistence of postures after
pronator drift testing, more sustained on the left.
Segment 3. Praxis testing with persistence of endtask postures on the left.
Segment 4. Interview with patient regarding posturing.

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Movement Disorders, Vol. 8, No. 1 , 1993